Gamal Badra

Helicobacter pylori infection in hepatic encephalopathy: Relationship to plasma endotoxins and blood ammonia

Background/Aim:  Hepatic encephalopathy (HE) is frequently observed in patients with advanced liver disease and manifests a wide variety of neuropsychiatric signs and symptoms. Ammonia toxicity and bacterial endotoxins have been suggested as key determinants of HE onset whereas a role for Helicobacter pylori infection has not been established. We investigated the correlation between H. pylori infection and HE severity (evaluated through functional tests) in 60 outpatients with established liver cirrhosis and 20 non‐cirrhotic controls.

Helicobacter pylori and Hepatitis C virus coinfection in Egyptian patients

Introduction: Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver disease worldwide. It has been shown that Helicobacter pylori (H. pylori) plays an important role in chronic gastritis, peptic ulcer disease and gastric malignancies, and its eradication has been advocated. The association between H. pylori infection and liver cirrhosis in patients with hepatitis C virus has been documented in different parts of the world; nevertheless, no conclusive data is available in Egypt. Materials and Methods: In the present study, the status of H. pylori infection was sought in 90 patients with chronic HCV infection and in 66 HCV-free healthy controls. Results: The study showed that the H. pylori positivity was increased significantly (P = 0.03) in the HCV-infected patients when compared to that in healthy controls, where H. pylori infection was found in 50 (55.6%) out of 90 of the HCV-infected patients versus 26 (39.4%) out of 66 of the healthy controls. In HCV-infected patients, the prevalence of H. pylori infection was increased significantly (P = 0.04) from chronic active hepatitis to cirrhosis. H. pylori infection was present in 6/18 (33.3%), 10/21 (47.6%), 16/27 (59.3%), 18/24 (75.0%) patients with chronic active hepatitis, Child-Pugh score A, Child-Pugh score B and Child-Pugh score C, respectively. More importantly, the prevalence of H. pylori infection in HCV-infected patients was increased very significantly (P = 0.003) with increasing Meld (model for end-stage liver disease) score. The prevalence of H. pylori was documented in 9/28 (32.1%) patients with Meld score >10 and in 41/62 (66.1%) patients with Meld score >10. Conclusion: It may be stated that our results collectively reflect a remarkable increase in H. pylori prevalence with advancing hepatic lesions, and the eradication treatment may prove beneficial in those patients with chronic hepatitis C.

Significance of serum matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in chronic hepatitis C patients.

Liver fibrosis (LF), where the chronic HCV infection is a major cause, is a characteristic of chronic liver diseases. LF results from chronic damage to the liver in conjunction with the accumulation of ECM proteins. Matrix metalloproteinases (MMPs) and their specific inhibitors (TIMPs) are thought to play an essential role in the hepatic lesions. The available data concerning the circulating levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in chronic hepatitis C are not conclusive. Therefore, the present study was designed to seek the relationship between serum MMP-9, and TIMP-1 to liver status in chronic liver disease in fifty patients divided into three groups (chronic hepatitis, liver cirrhosis and hepatocellular carcinoma). MMP-9 and TIMP-1 were analyzed by the enzyme linked immunosorbent assay (ELISA). The results showed that the lowest serum level of MMP-9 was found in chronic hepatitis patients compared to the control ( P < 0.05). Serum MMP-9 is decreasing during progression of chronic hepatitis to cirrhosis showing the least level in the cirrhotic group. Serum TIMP-1 was significantly higher in the cirrhotic group compared to chronic hepatitis ( P < 0.05) and controls ( P < 0.001). MMP-9 was negatively correlated to both TIMP-1 and the histological severity in chronic hepatitis. There was a positive correlation between TIMP-1 and the degree of fibrosis (r = 0.73, P < 0.001). Lastly, there was a statistically significant increase of MMP-9 ( P < 0.001) and TIMP-1 ( P < 0.05) in HCC patients compared with the other groups. In conclusion, these findings raise the possibility of using serum TIMP-1 as a non-invasive assay in liver fibrosis. Further, the altered balance between circulating MMP-9 and TIMP-1 during HCV infection may play an important role in aggravating liver injury progression in chronic liver diseases.

Differences in phosphatidylcholine and bile acids in bile from Egyptian and UK patients with and without cholangiocarcinoma

BACKGROUND Cholangiocarcinoma (CC) is a fatal malignancy, the incidence of which is increasing worldwide, with substantial regional variation. Current diagnostic techniques to distinguish benign from malignant biliary disease are unsatisfactory. Metabolic profiling of bile may help to differentiate benign from malignant disease. No previous studies have compared the metabolic profiles of bile from two geographically and racially distinct groups of CC patients. OBJECTIVES This study aimed to compare metabolic profiles of bile, using in vitro proton magnetic resonance spectroscopy, from CC patients from Egypt and the UK, and from patients with CC and patients with non-malignant biliary disease. METHODS A total of 29 bile samples, collected at cholangiography, were analysed using an 11.7-T system. Samples were from eight CC patients in either Egypt (n = 4) or the UK (n = 4) and 21 patients with benign biliary disease (choledocholithiasis [n = 8], sphincter of Oddi dysfunction [n = 8], primary sclerosing cholangitis [n = 5]). RESULTS Bile phosphatidylcholine (PtC) was significantly reduced in CC patients. Egyptian CC patients had significantly lower biliary PtC levels compared with UK patients. Taurine- and glycine-conjugated bile acids (H-26 and H-25 protons, respectively) were significantly elevated in bile from patients with CC compared with bile from patients with benign diseases (P = 0.013 and P < 0.01, respectively). CONCLUSIONS Biliary PtC levels potentially differentiate CC from benign biliary disease. Reduced biliary PtC in Egyptian compared with UK patients may reflect underlying carcinogenic mechanisms.

Allopurinol vs octreotide in the prevention of post-ERCP pancreatitis in patients with biliary obstruction. A randomized controlled trial

Allopurinol vs octreotide in the prevention of post-ERCP pancreatitis in patients with biliary obstruction. A randomized controlled trial

Serum islet cell autoantibodies during interferon α treatment in patients with HCV-genotype 4 chronic hepatitis

Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver disease worldwide and HCV genotype 4 (HCV4) is predominant in African and Middle Eastern countries. It is well established that interferon-α (IFNa) treatment for HCV may trigger serum autoantibodies against pancreatic islet cells (ICA) in a subgroup of patients. Available data on the incidence of ICA during IFNa therapy for chronic HCV4 infection are not conclusive. We investigated the appearance of ICA in 40 naïve Egyptian patients (38 males, 32 ± 6 years) with histologically defined chronic HCV4 infection undergoing IFNa treatment at a dose of 9-million U/week for 24 weeks. Serum samples were collected at baseline and following IFNa therapy and ICA were detected using indirect immunofluorescence. Baseline evaluation indicated that 2/40 (5%) patients had detectable serum ICA. After the completion of the treatment scheme, 12/38 (32%) previously ICA negative patients became ICA positive; however, no patient developed impaired glucose tolerance (IGT) or diabetes during follow-up. In conclusion, we submit that IFNa treatment for chronic hepatitis C (CHC) may induce serum ICA in one-third of Egyptian patients with HCV4. These autoantibodies, however, do not lead to alterations in glucose metabolism.

Long-term effect of mass chemotherapy of Schistosoma mansoni on infection rate and diagnosis accuracy

OBJECTIVES To assess the performance of microscopic stool examination, which is used widely for the diagnosis and assessment of infection rates of Schistosoma mansoni in Egypt, for the evaluation of chemotherapy efficacy after a decade of regular mass treatment. METHODS A total of 651 individuals from Lower Egypt (55 children and 596 adults) were examined for S. mansoni ova by microscopic stool examination (MSE) alone (n=166; 111 adults and 55 children), rectal biopsy (RB) alone (n=32 adults), or both MSE and RB (n=453 adults). RESULTS Infection detection rates were significantly lower in the MSE alone group (9%; 15/166) compared to the RB alone group (40.6%; 13/32) and to the RB+MSE group (37.7%; 171/453). Out of all positive cases in the MSE+RB group, only 23/171 patients (13.5%) were positive by stool examination, of whom 21 were also positive by RB, in contrast to 169/171 patients (86.5%) positive by RB in the same group. It was noted that adding MSE to RB did not increase the prevalence compared to RB alone: 37.3% in the MSE+RB group vs. 40.6% in the RB only group. Using the summation of both MSE and RB tests as the gold standard, the sensitivity of MSE was significantly lower than that of RB: 13.5% vs. 98.8%. CONCLUSIONS The implementation of mass treatment programmes has resulted in a new era of light infection, for which conventional parasitological methods for the diagnosis and monitoring of infection can miss many patients.

Proteomic Patterns in Serum and Urine of Patients Infected with Schistosoma mansoni: Basis for New Biomarker

Diagnosis of S. mansoni infection is carried out by the detection of eggs in faeces. This method has low sensitivity, especially with patients in the acute phase of the illness or with low-intensity infection. Serological tests cannot differentiate between active and past infection. Non-invasive diagnostic tests for active disease and monitoring response to treatment are required. This study was performed to identify serum and urine proteomic based biomarkers in patients with S. mansoni infection before and after therapeutic intervention using Surface Enhanced Laser Desorption/Ionization Time of Fight-Mass Spectrometry (SELDI TOF-MS). Serum samples were collected from 30 patients and urine samples from another15 patients both prior to and four to six weeks after treatment with praziquantel. All patients had a confirmed diagnosis of active infection on rectal biopsy. Serum and urine proteomic profiles were obtained by SELDI TOF-MS using cation capture (CM10) and immobilized metal affinity (IMAC30) ProteinChip ™ arrays. In urine samples, nine protein peaks demonstrated significant differences between pre and post treatment samples: 46 kDa, 44 kDa, 34 KDa, 13.3 KDa, 10.8 KDa, 19.7 kDa, 15.9 kDa, 18.1 kDa, 4.7 KDa (All had p<0.05). On ROC curve analysis, only the protein at 4.7 kDa showed a significant diagnostic signal (AUROC=0.77) indicating that it has potential as biomarker for active infection. In serum samples, only four peaks were found to be significantly different between pre and post treatment groups (p value<0.01). However no serum peak demonstrated significance on ROC curve analysis. These results suggest that urinary proteomic testing may provide a non-invasive diagnostic test for S. mansoni.